Content includes Physiology of sleep and and its correlation with EEG waves along with specific characteristics of different phases of sleep as well as an account of sleep disorders.
Understanding the sleep cycle is often the first step to better sleep quality. When you know, what affects your sleep cycle, you can take measures to cut out distractions and get ample restful sleep every night.
Also, to help you understand the various sleep stages and sleep cycles easily, we have also created an infographic for this.
Read more details on the source site: https://sleepsherpa.com/stages-of-sleep-and-sleep-cycles-explained/
The outcome of this course is for the learner to describe the normal stages of sleep, common sleep measurement tools sleep characteristic, common sleep disorders, the changes that affect the quality and quantity of sleep as an individual ages, and methods the healthcare provider can use to assess and assist clients with sleep disorders.
Sleep is defined as unconsciousness from which the person can be aroused by sensory or other
stimuli.
distinguished from coma, which is unconsciousness from which the person cannot be
aroused. There are multiple stages of sleep, from very light sleep to very deep sleep; sleep
researchers also divide sleep into two entirely different types of sleep that have different qualities,
Sleep-wake cycle refers to our 24 hour daily sleep pattern which consists of
approximately 16 hours of daytime wakefulness and 8 hours of night-time sleep.
The complex process of the sleep-wake cycle is controlled by the body’s circadian rhythm and sleep homeostasis (the amount of accumulated sleep need that builds during time spent awake).
Understanding the sleep cycle is often the first step to better sleep quality. When you know, what affects your sleep cycle, you can take measures to cut out distractions and get ample restful sleep every night.
Also, to help you understand the various sleep stages and sleep cycles easily, we have also created an infographic for this.
Read more details on the source site: https://sleepsherpa.com/stages-of-sleep-and-sleep-cycles-explained/
The outcome of this course is for the learner to describe the normal stages of sleep, common sleep measurement tools sleep characteristic, common sleep disorders, the changes that affect the quality and quantity of sleep as an individual ages, and methods the healthcare provider can use to assess and assist clients with sleep disorders.
Sleep is defined as unconsciousness from which the person can be aroused by sensory or other
stimuli.
distinguished from coma, which is unconsciousness from which the person cannot be
aroused. There are multiple stages of sleep, from very light sleep to very deep sleep; sleep
researchers also divide sleep into two entirely different types of sleep that have different qualities,
Sleep-wake cycle refers to our 24 hour daily sleep pattern which consists of
approximately 16 hours of daytime wakefulness and 8 hours of night-time sleep.
The complex process of the sleep-wake cycle is controlled by the body’s circadian rhythm and sleep homeostasis (the amount of accumulated sleep need that builds during time spent awake).
This is very simple and very useful for the students of medical and nursing students .it will help you in enhancing your knowledge.i will be happy if you like and share my ppt
it explain about definition of sleep, normal sleep, sleep disturbance, causes of sleep disturbance, management therapy, nursing therapy and its effect om normal life.
lecture 24 from a college level introduction to psychology course taught Fall 2011 by Brian J. Piper, Ph.D. (psy391@gmail.com) at Willamette University, includes sleep stages, EEG, development, dreams, purpose of sleep
Similar to Physiology of Sleep and its correlation with EEG waves (20)
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
2. • Sleep ,Unconsciousness from which the
person can be aroused by sensory or other
stimuli.
• Coma, which is unconsciousness from which
the person cannot be aroused.
3. Two Types of Sleep
• (1) slow-wave sleep,
• because in this type of sleep the brain waves
are very strong and very low frequency,
• (2) rapid eye movement sleep (REM sleep),
• because in this type of sleep the eyes undergo
rapid movements despite the fact that the
person is still asleep.
4. • Most sleep during each night is of the slow-wave
variety; this is the deep, restful sleep that the
person experiences during the first hour of sleep
after having been awake for many hours.
• REM sleep, occurs in episodes that occupy about
25 per cent of the sleep time in young adults;
each episode normally recurs about every 90
minutes.
• This type of sleep is not so restful, and it is
usually associated with vivid dreaming.
5. Slow-Wave Sleep
• Decrease in both peripheral vascular tone and many
other vegetative functions of the body.
• There are 10 to 30 per cent decreases in blood
pressure, respiratory rate, and basal metabolic rate.
• Although slow-wave sleep is frequently called
“dreamless sleep,” dreams and sometimes even
nightmares do occur during slow-wave sleep.
• Dreams of slow-wave sleep usually are not
remembered.
• Consolidation of the dreams in memory does not
occur.
6.
7. REM Sleep (Paradoxical Sleep,
Desynchronized Sleep)
• In a normal night of sleep, bouts of REM sleep
lasting 5 to 30 minutes usually appear on the
average every 90 minutes.
8. Important characteristics of REM
sleep
• 1. It is usually associated with active dreaming and
active bodily muscle movements.
• 2. The person is even more difficult to arouse by
sensory stimuli than during deep slow-wave sleep, and
yet people usually awaken spontaneously in the
morning during an episode of REM sleep.
• 3. Muscle tone throughout the body is exceedingly
depressed, indicating strong inhibition of the spinal
muscle control areas.
• 4. Heart rate and respiratory rate usually become
irregular, which is characteristic of the dream state.
9. • Irregular muscle movements do occur.
• These are in addition to the rapid movements of
the eyes.
• The brain is highly active in REM sleep, and
overall brain metabolism may be increased as
much as 20 per cent.
• This type of sleep is also called paradoxical sleep
because it is a paradox that a person can still be
asleep despite marked activity in the brain.
10. • Occurrence of large phasic potentials that
originate in the cholinergic neurons in the
pons and pass rapidly to the lateral geniculate
body and from there to the occipital cortex.
They are called pontogeniculo-occipital (PGO)
spikes.
11. • Positron emission tomography (PET) scans of
humans in REM sleep show increased activity
in the pontine area, amygdala, and anterior
cingulate gyrus, but decreased activity in the
prefrontal and parietal cortex.
• Activity in visual association areas is
increased, but there is a decrease in the
primary visual cortex.
12. • Organisms in REM sleep suspend
central homeostasis, allowing large
fluctuations in respiration, thermoregulation,
and circulation which do not occur in any
other modes of sleeping or waking.
• The body abruptly loses muscle tone, a state
known as REM atonia.
13.
14. Basic Theories of Sleep
• An earlier theory of sleep was that the
excitatory areas of the upper brain stem, the
reticular activating system, simply fatigued
during the waking day and became inactive as
a result. This was called the passive theory of
sleep.
15. Sleep Is Believed to Be Caused by an
Active Inhibitory Process.
• There seems to be some center located below
the midpontine level of the brain stem that is
required to cause sleep by inhibiting other
parts of the brain.
16. • Neuronal Centers, Neurohumoral Substances,
and Mechanisms That Can Cause Sleep— A
Possible Specific Role for Serotonin
• Stimulation of several specific areas of the
brain can produce sleep with characteristics
near those of natural sleep.
17. • 1. The most conspicuous stimulation area for
causing almost natural sleep is the raphe nuclei in
the lower half of the pons and in the medulla.
• These nuclei are a thin sheet of special neurons
located in the midline.
• Nerve fibers from these nuclei spread locally in
the brain stem reticular formation and also
upward into the thalamus, hypothalamus, most
areas of the limbic system, and even the
neocortex of the cerebrum.
18. • Many nerve endings of fibers from these
raphe neurons secrete serotonin.
• When a drug that blocks the formation of
serotonin is administered to an animal, the
animal often cannot sleep for the next several
days.
• Therefore, it has been assumed that serotonin
is a transmitter substance associated with
production of sleep.
19.
20. • 2. Stimulation of some areas in the nucleus of
the tractus solitarius can also cause sleep.
• 3. Stimulation of several regions in the
diencephalon can also promote sleep,
including
• (1) the rostral part of the hypothalamus,
mainly in the suprachiasmal area
• (2) an occasional area in the diffuse nuclei of
the thalamus.
21. • Lesions in Sleep-Promoting Centers Can
Cause Intense Wakefulness.
• Discrete lesions in the raphe nuclei lead to a
high state of wakefulness.
• This is also true of bilateral lesions in the
medial rostral suprachiasmal area in the
anterior hypothalamus.
22. • In both instances, the excitatory reticular
nuclei of the mesencephalon and upper pons
seem to become released from inhibition,
thus causing the intense wakefulness.
• Indeed, sometimes lesions of the anterior
hypothalamus can cause such intense
wakefulness that the animal actually dies of
exhaustion.
23. • muramyl peptide, a low-molecular-weight
substance that accumulates in the
cerebrospinal fluid and urine in animals kept
awake for several days.
24. Possible Cause of REM Sleep.
• Why slow-wave sleep is broken periodically
by REM sleep is not understood.
• However, drugs that mimic the action of
acetylcholine increase the occurrence of REM
sleep.
25. Cycle Between Sleep and Wakefulness
• When the sleep centers are not activated, the
mesencephalic and upper pontile reticular
activating nuclei are released from inhibition,
which allows the reticular activating nuclei to
become spontaneously active.
• This in turn excites both the cerebral cortex and
the peripheral nervous system, both of which
send numerous positive feedback signals back to
the same reticular activating nuclei to activate
them still further.
26.
27. Physiologic Effects of Sleep
• We might postulate that the principal value of
sleep is to restore natural balances among the
neuronal centers.
• The specific physiologic functions of sleep
remain a mystery, and they are the subject of
much research.